Exam review

GIT and Liver, Gall bladder

LiverHepatitis

Circulatory diseases

Hepatitis

Hepatitis A infection (infectious hepatitis) : RNA virus

Spread: Fecal-oral route. C/F: Never develop a carrier, chronic state , Hepatocellular carcinoma.

C/F: Mild disease, quick recovery, Acute disease: Positive for IgM antibody to hepatitis A virus (antigen).

Incidence: Sporadic outbreaks in restaurants.In places with poor hygiene. Common in childrenAdults are often seropositive

Hepatitis B infection (DNA virus)

Spread: Parenterally and by intimate contact through mucosal surfaces.

Vertical transmission is common.

Carrier state is common, Less chance of Chronic hepatitis, cirrhosis. Increased chance of Developing Hepatocellular carcinoma.Carrier: Positive HBsAg even after 6 months, with normal health but can transmit infection.

Interpretation of HBV serology

Acute phase Carrier phase Chronic

HBsAg + IgM Anti-HBs.

HBsAg +> 6 months

No surface antigen*

HBcAg + IgM Anti-HBc

IgGAnti-HBc > 6

months

IgGAnti-HBc > 6 months

DNA polymerase/ HBV DNA

HBV DNA HBV DNA

Hepatitis C infection (non-A, non-B hepatitis)RNA virus

Spread : Parenterally and via contact-associated mechanisms.Vertical transmission is NOT common. C/F : More chance of Chronic hepatitis cirrhosis and Hepatocellular carcinoma.Acute disease: Positive for IgM antibody to hepatitis C virus antigen.Chronic disease: Positive for IgG antibody to hepatitis C virus (antigen). Fatty change seen.Incidence: It is seen most commonly in the homosexual community, intravenous drug users, and patients who have received multiple blood transfusions.

Delta virus infectionRNA virus that is replication defective : cause

infection when encapsulated by HBsAgCo-infection : Positive for IgM antibody to hepatitis D virus antigen and IgM antibody to HBc antigen.Super infection: Positive for IgM antibody to hepatitis D virus antigen and HBsAg.Incidence: common in drug addict and hemophiliacClinical features: Fulminant hepatitis common with this infection, cirrhosis.

Acute HepatitisLiver cell swelling, feathery degeneration

Ground glass Hepatocytes and sanded nuclei and apoptosis (HBV).

Chronic hepatitis

Symptomatic, biochemical and/or serologicalevidence of relapsing hepatic disease for more than 6 months.Etiology: HCV ( commonest )A. General features

A. Bridging necrosis and fibrosisB. Lymphoid aggregatesC. Piecemeal necrosis= interface hepatitis

Circulatory disorders of liver

These are the disease due to circulatory disturbances

Disturbance of circulation within the liver: Cirrhosis, sinusoidal dilatation, veno occlusive disease.

Disturbance of circulation Out side the liver : Shock, RHF, hepatic artery thrombosis (cause infarct), portal vein thrombosis, hepatic vein thrombosis.

Disease

• Sinusoidal dilation (aka)= Peliosis hepatis– Etiology : Anabolic steroid , danazol, OC

pill – Peliotic lesions usually disappear after

cessation of drug treatment. • Nutmeg liver/ centrilobular necrosis/

cardiac cirrhosis– Etiology : Right sided heart failure/shock

Nutmeg liver and centrilobular necrosis

Budd-Chiari syndromeDef: acute thrombotic occlusion of the hepatic vein.Etiology;

1. Polycythemia Vera2. Myeloproliferative disorder (CML)3. Use of OC pill, HCC. 4. Deficiencies in antithrombin, protein S, or

protein C, or mutations of factor V Clinical: Tender hepatomegaly, some features of PHT,

liver enzyme elevation.

Diagnostic procedure: venogram

Veno occlusive diseases (VOD)

Etiology : Immediate week after bone marrow transplantation with immunosuppressant therapy.

Pathogenesis :Fibrosis of Small hepatic vein radicles.

Clinical:tender hepatomegaly, ascites, weight gain, and jaundice

Liver infarct

• Cause:– thrombosis or compression of an intrahepatic

branch of the hepatic artery by embolism, neoplasia,sepsis.

Portal Vein Obstruction and Thrombosis

• Insidious and well tolerated • Morphology: Well demarcated area of red-

blue discoloration (infarct of Zahn), no necrosis only atrophy.

• Ascites and other manifestations of portal hypertension

Drug and toxin induces liver disease

Type of Hepatobiliary damage

Drug or toxin

Micro vesicular fatty change

Tetracycline, ethanol

Macro vesicular fatty change

Ethanol, Methotrexate and diabetes mellitus

Centrilobular necrosis Acetaminophen, halothane.

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